Congestive heart failure in normotensive man. Haemodynamics, renin, and angiotensin II blockade.

Turini, G. A.; Brunner, Hans R.; Ferguson, Roger K.; Rivier, J.-L.; Gavras, Haralambos

doi:10.1136/hrt.40.10.1134

Cited by 71 publications

(10 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although initially known for its vasoconstrictive action, the adverse effects of ANG II elevation on the heart independent of its hemodynamic influence were recognized in the early 1970s (7,16), and the cardioprotective outcomes of the pharmacological interventions that either prevent the ANG II formation from the inactive angiotensinogen precursor (14) or inhibit its interaction with specific receptors (15,48) are now well appreciated in clinical practice (6,13,17).…”

mentioning

confidence: 99%

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Schwartz¹,

Duka²,

Duka³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Schwartz, Faina, Arvi Duka, Irena Duka, Jing Cui, and Haralambos Gavras. Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression. Am J Physiol Heart Circ Physiol 287: H1957-H1966, 2004. First published July 8, 2004 doi:10.1152/ajpheart.00568.2004.-Although the central role of ANG II in cardiovascular homeostasis is well appreciated, the molecular circuitry of its many actions is not completely understood. With the use of serial analysis of gene expression to assess global transcriptional changes in the heart of mice after continuous 7-day ANG II administration, we identified patterns of gene expression indicative of cardiac remodeling, including coordinate regulation of genes previously described in a context of processes associated with hypertrophy and fibrosis. In addition, we discovered several novel ANG II targets, including characterized genes of known function, recently annotated genes of unknown function, and the putative genes not yet present in current databases. The serial analysis of gene expression approach to assess the role of ANG II presented in this report provides new venues for inquiries into ANG II-mediated cardiac function.genome-wide transcriptional profiling; hypertension; cardiac remodeling; hypertrophy; fibrosis THE KEY ROLE of ANG II in cardiovascular homeostasis is well documented. Although initially known for its vasoconstrictive action, the adverse effects of ANG II elevation on the heart independent of its hemodynamic influence were recognized in the early 1970s (7, 16), and the cardioprotective outcomes of the pharmacological interventions that either prevent the ANG II formation from the inactive angiotensinogen precursor (14) or inhibit its interaction with specific receptors (15, 48) are now well appreciated in clinical practice (6,13,17).Experimental animal studies have shown that ANG II administration can cause multifocal myocardial lesions (16, 47), and, via ANG II type 1 receptors, directly induce cardiac remodeling that involves myocyte hypertrophy (9, 25), fibroblast proliferation, and subsequent fibrosis (47), thus leading to the development of pathological cardiac hypertrophy and, ultimately, heart failure. Both in vivo and in vitro studies revealed that the ANG II effects in the heart are accompanied by changes in gene expression in the cardiac myocytes, fibroblasts, and endothelial cells (24). While the queries of selected ANG II targets supplied important information on several molecular pathways underlying the physiological and pathophysiological actions of ANG II, an all-inclusive view is provided by the genome-wide transcriptional profiling that offers an opportunity to connect separate pieces of the puzzle through the identification of the new players not intuitively obvious from our present understanding of physiology. Thus simultaneous evaluation of 4,000 genes by the use of microarray technology to query the quantitative changes in left ventricular RNA in response to ANG II-induced progression, and, subsequently, regre...

show abstract

mentioning

confidence: 99%

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Schwartz¹,

Duka²,

Duka³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

show abstract

“…Thus, direction and amplitude of the response of both mean blood pressure and total peripheral resistance to [Sar1, He8] All appeared to be practically dependent on basal PRA levels, probably endogenous All levels, in hyper tensive patients. The association of reduced blood pressure and total peripheral resistance with no change in cardiac output during [Sar1, Ala8] All infusion also has been reported in normotensive patients with congestive heart failure and increased PRA (24). None of our patients, how ever, had any evidence of heart failure.…”

Section: Discussionmentioning

confidence: 71%

Hemodynamic Effects of [Sar<sup>1</sup>, Ile<sup>8</sup>] All, an Angiotensin II Analog, in the Renin Subgroups of Essential Hypertension

Morimoto¹,

Yamamoto²,

Uchida³

et al. 1981

Cardiology

View full text Add to dashboard Cite

Hemodynamic effects of [Sar¹, Ile⁸] All, an angiotensin II analog, were studied in 30 patients with essential hypertension, who were subdivided into 11 low renin, 10 normal renin and 9 high renin groups according to low, normal and high PRA values both before and after furosemide administration (80 mg, orally) plus 4 h of ambulation, respectively. [Sar¹, Ile⁸] All infusion (600 ng/kg/min) produced significant increases in mean blood pressure (MBP) and total peripheral resistance index (TPRI) in normal renin and low renin groups and significant decreases in MBP and TPRI in high renin group, while the cardiac index and heart rate remained unchanged during the infusion in these three groups. Change in MBP at 30 min of [Sar¹, Ile⁸] All infusion correlated significantly with alteration in TPRI in 23 patients with essential hypertension, who completed the 30-min infusion. The response of both MBP and TPRI to [Sar¹, Ile⁸] All also correlated significantly with basal PRA. These results suggest that blood pressure response to [Sar¹, Ile⁸] All in essential hypertension is primarily due to alteration in total peripheral resistance and that direction and amplitude of the response of both MBP and TPRI are practically dependent on basal PRA levels.

show abstract

“…Activation of the renin-angiotensin-aldosterone system has been related to the raised systemic vascular resistance and increase in plasma volume that occur in heart failure, plasma renin activity being increased or inappropriately normal (Brown et al, 1970;Genest et al, 1968;Haber, 1976;Turini et al, 1978: Vandongen & Gordon., 1970. Inhibition of angiotensin-converting enzyme with oral captopril has been shown to increase cardiac output and reduce left ventricular filling pressure in patients with heart failure, and the symptomatic and haemodynamic benefits of captopril appear to be maintained with long-term treatment (Ader et al, 1980;Dzau et al, 1980;Levine et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Clinical and haemodynamic effects of low dose captopril in severe chronic heart failure.

Sharpe¹,

Coxon²

1982

Brit J Clinical Pharma

View full text Add to dashboard Cite

1 The clinical and haemodynamic effects of low doses of the oral converting‐enzyme inhibitor captopril were studied in 18 patients with severe chronic heart failure. Increasing doses of 1 mg, 2.5 mg, 6.25 mg, 12.5 mg, and 25 mg captopril were given at two hour intervals with haemodynamic monitoring. Graded haemodynamic improvement (increased stroke volume index and reduced mean pulmonary capillary wedge pressure) occurred from one hour with reduction of blood pressure closely associated. 2 Maximal haemodynamic improvement for the group was seen at six and seven hours after the 6.25 mg and 12.5 mg doses, when stroke volume index was increased by 35% and mean pulmonary capillary wedge pressure reduced by 40% from control. Captopril 12.5 mg‐ 50 mg eight hourly was continued long‐term but withdrawn in two patients with symptomatic hypotension and one patient with altered taste. 3 Four patients died and one was non‐compliant with therapy. At three months 10 patients showed significant improvement in symptoms, treadmill exercise duration, and echocardiographic indices of left ventricular size and function. The results of repeat haemodynamic measurements were similar to optimal measurements obtained during the initial study. 4 At two years six patients remained alive, five having maintained their symptomatic improvement. Thus small doses of captopril produce haemodynamic improvement in heart failure with a closely associated reduction of blood pressure. Symptomatic and haemodynamic benefit is maintained with long‐term treatment.

show abstract

Congestive heart failure in normotensive man. Haemodynamics, renin, and angiotensin II blockade.

Cited by 71 publications

References 36 publications

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Novel targets of ANG II regulation in mouse heart identified by serial analysis of gene expression

Hemodynamic Effects of [Sar<sup>1</sup>, Ile<sup>8</sup>] All, an Angiotensin II Analog, in the Renin Subgroups of Essential Hypertension

Clinical and haemodynamic effects of low dose captopril in severe chronic heart failure.

Contact Info

Product

Resources

About